Neuropeptides such as calitonin gene-related product (CGRP) and substance P are released from the peripheral nerve terminals of capsaicin-sensitive after tissue injury or during inflammation. Numerous studies suggest that the release of neuropeptides enhances the inflammatory effect (neurogenic inflammation)and regulates wound healing. Our preliminary studies indicate that epinephrine and beta- adrenergic receptors inhibit neuropeptide release. Therefore we want to determine 1)which beta-adrenergic receptor subtypes are responsible for this effect 2)if beta-adrenergic agonist are acting directly on the sensory nerve terminal 3) whether sympathetic innervation is required to see beta-adrenergic modulation of neuropeptide release. To perform these studies, we will use a rat dental pulp model as pulpal tissue is heavily innervated with both sensory nerve fibers and contain sympathetic fibers as well. These studies will further our knowledge of sympathetic interactions during pain and inflammation.